Novel active fixation lead guided by electrical delay can improve response to cardiac resynchronization therapy in heart failure

Cardiac resynchronization therapy (CRT) for heart failure (HF) recently has shown optimal results by targeting electrically delayed sites in coronary sinus (CS) branches. However this purpose often cannot be reached because of unstable left ventricular (LV) lead position. In current study were assessed the long-term effects of the novel active fixation LV lead in CS, guided by electrical delay (QLV), in patients with HF due to coronary artery disease. Methods One hundred eighty-five consecutive patients underwent CRT with intraoperative evaluation of QLV in the target position of the LV lead. When the novel active fixation LV lead was available, 98 consecutive patients received it, composing the Fix group. They were compared with 87 patients with a conventional passive fixation lead (No Fix group). The final LV lead position was assessed by fluoroscopy. Clinical response to CRT was assessed within a period of about 3 years: patients experiencing HF rehospitalization and death due to HF were defined as non-responders. Results There were no significant differences between groups in the final position of LV lead in left anterior oblique view (Pearson χ2 = 0.12; P = 0.73). In right anterior oblique view, a basal position was reached more in the Fix group (38%) than in the No Fix group (6.5%) (Pearson χ2 = 23.095; P < 0.001). QLV was significantly greater in the Fix group (122.6 ± 33.2 ms; SE = 3.6) than in the No Fix group (97.5 ± 37.8 ms; SE = 4.9) (t = 4.17; P < 0.001). Rehospitalizations for HF were 37 in the No Fix group and 14 in the Fix group. Deaths due to HF were 49 in the No Fix group and 18 in the Fix group. Survival analysis, assessed by Cox regression, showed that the Fix group had a better outcome both for HF rehospitalizations [hazard ratio (HR) = 0.48; 95% confidence interval (CI) = 0.25–0.9; P = 0.023] and death due to HF (HR = 0.55; 95% CI = 0.31– 0.97; P = 0.04) in comparison with the No Fix group. Adjustment for baseline characteristics by multivariate analysis showed that an active fixation lead in CS, as a covariate, was still significant both for HF rehospitalizations (HR 0.46; 95% CI = 0.24–0.88; P = 0.019) and for death due to HF (HR 0.5; 95% CI = 0.28–0.9; P = 0.021). Conclusions The novel active fixation LV lead allowed to target sites with greater QLV. Often maximum QLV was documented in basal segments, were stability of conventional passive fixation leads is not enough. Patients receiving it experienced less HF rehospitalizations and less death due to HF. Active fixation lead in CS guided by QLV can improve long-term prognosis in patients with HF due to coronary artery disease undergoing to CRT.